Aberrant glycosylation in IgA nephropathy (IgAN)

被引：144
|
作者：
Coppo, R [1 ]
Amore, A [1 ]
机构：
[1] Osped Regina Margherita, I-10126 Turin, Italy
来源：
KIDNEY INTERNATIONAL | 2004年 / 65卷 / 05期
关键词：
IgA nephropathy; aberrantly glycosylated IgA; pathogenesis of glomerular diseases;
D O I：
10.1111/j.1523-1755.2004.05407.x
中图分类号：
R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];
学科分类号：
1002 ; 100201 ;
摘要：
Immunoglobulin A nephropathy (IgAN) patients exhibit circulating IgA1 with reduced galactose (Gal) and/or sialic acid (Neu5Ac) and increased exposure of N-acetylgalaclosamine (GalNAc). These IgA glycoforms fix complement and in mesangial cells regulate integrin expression, enhance nitric oxide synthase (NOS) activity, decrease endothelial growth factor synthesis, meanwhile depressing proliferation and increasing apoptotis. Drugs can be targeted to the effects enhanced by aberrantly glycosylated IgA1 on mesangial cells. Recent data suggest that aberrant IgA1 glycosylation may modulate clinical expression and progression of IgAN.
引用
收藏
页码：1544 / 1547
页数：4
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